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. 2019 Dec 29;21(2):e47895. doi: 10.15252/embr.201947895

Figure 6. HO‐1 deficiency in the niche causes exhaustion of LT‐HSCs.

Figure 6

  • A
    Deletion of HO‐1 in myeloid lineage did not cause expansion of LT‐HSCs and did not alter their cell cycle status.
  • B
    Scheme of the experiment assessing long‐term effect of HO‐1‐deficient niche on function of HSCs.
  • C
    Long‐term PB chimerism derived from HSCs transplanted to HO‐1−/− recipients is lower than from HSCs transplanted to HO‐1+/+ recipients. *P < 0.05, 2‐way ANOVA. Data are shown as mean ± SEM, n = 5–12/group.
  • D, E
    (D) Chimerism among BM HSPC fractions and (E) total number of cells derived from HSCs transplanted to HO‐1−/− recipients are lower than from HSCs transplanted to HO‐1+/+ recipients. Data are shown as mean ± SEM, n = 5–12/group.
  • F
    HSCs that were initially transplanted to primary HO‐1−/− recipients did not reconstitute secondary HO‐1+/+ recipients, in contrast to HSCs that were initially transplanted to HO‐1+/+ recipients, n = 5–12/group.
  • G
    Scheme of the experiment assessing short‐term homing of HSPC to HO‐1‐deficient niche.
  • H
    Short‐term homing of HSPC to HO‐1+/+ or HO‐1−/− BM did not differ. Data are shown as mean ± SEM, n = 5/group, unpaired t‐test.